The present invention relates to cardial pacing systems, and, in particular, to cardial pacing systems providing for the immediate contractual stimulation of an atrium of a mammalian heart upon the detection of a premature atrial contraction in a second atrium.
The cardiovascular system provides oxygenated blood to various structures of the body. In a normally functioning heart, the body""s demand for oxygenated blood varies, and the heart responds by increasing or decreasing its rate and force of contraction to meet the demand. An electrical signal generated by the sinus node in the upper right atrial wall near the base of the heart is transmitted through the two upper heart chambers, i.e., the right and left atria, which causes them to synchronously contract. The contraction of the two upper heart chambers forces blood, pooled within the chambers, through open heart valves and into the right and left ventricles, the two lower heart chambers. The atrial electrical depolarization wave arrives at the atrio-ventricular (AV) node, superior to the ventricles, and triggers the conduction of a ventricular depolarization wave down the bundle of His in the septum between the right and left ventricles to the apex of the heart. The two ventricles contract after a brief AV delay time following the sinus node depolarization as the depolarization wave then advances superiorly, posteriorly, and anteriorly throughout the outer ventricular wall of the heart. The two lower heart chambers contract and force the blood through the vascular system of the body. The contraction of the right and left ventricles then proceeds in an organized fashion which optimizes the emptying of the ventricular chambers. The synchronous electrical depolarization of the atrial and ventricular chambers can be electrically sensed and displayed, and the electrical waveform is characterized by accepted convention as the xe2x80x9cPQRSTxe2x80x9d complex. The PQRST complex includes the P-wave, which corresponds to the atrial depolarization wave; the R-wave, corresponding to the ventricular depolarization wave; and the T-wave, which represents the re-polarization of the cardiac cells.
Various disease mechanisms may cause conduction disturbances which interfere with the natural conduction system of the heart and affect the heart""s ability to provide adequate cardiac output to the body. In certain disease mechanisms, the sinus node may fail to depolarize and commence the P-wave as rapidly as required to satisfy the demand for oxygenated blood, or the atria themselves may spontaneously depolarize at rates that are well in excess of the ability of the ventricles to respond. In such situations, the ventricles may compensate by depolarizing spontaneously from ectopic depolarization sites. In other cases in which the sinus node operates correctly, 1:1 atrial and ventricular depolarization synchrony is lost because the AV node may fail to respond to the P-waves or a defect in the bundle of His interferes with the conduction of the ventricular depolarization. In these cases, the ventricles may contract at a rate inadequate for providing sufficient cardiac output.
When either the atria or ventricles contract too slowly, the patient may be a candidate for implantation of a cardiac pacemaker for restoring the heart rate by applying pacing pulses to the heart chamber that is malfunctioning at a pacing rate that restores adequate cardiac output. Modern implantable cardiac pacemakers comprise an implantable pulse generator (IPG) and a lead or leads extending from the IPG to pace/sense electrode or electrodes located with respect to the heart chamber to deliver the pacing pulses and/or sense the P-wave or R-wave. Typically, the leads are transvenously introduced into the particular heart chamber via the superior vena cava and right atrium, and the pace/sense electrodes are maintained in contact with the heart tissue by a fixation mechanism at the distal end of the lead. However, leads may be placed subcutaneously between the IPG and the exterior or the heart, and the pace/sense electrodes attached to the epicardium at the desired sites. Moreover, enocardial coronary sinus leads are introduced through the right atrium into the coronary sinus and the great vein to locate pace/sense electrodes in proximity to the left atrium or the left ventricle.
A single chamber, demand pacemaker may be implanted into the patient to supply pacing pulses to a single upper or lower heart chamber, typically the right atrium or right ventricle, in response to bradycardia of the same chamber. In an atrial demand pacemaker operating in an AAI pacing mode, an atrial pacing pulse is delivered to the atrial pace/sense electrodes by the IPG if a P-wave is not sensed by an atrial sense amplifier coupled to the artial pace/sense electrodes within an atrial escape interval (A-A interval) timed by an atrial escape interval timer. In a ventricular demand pacemaker operating in a VVI pacing mode, a ventricular pacing pulse to the ventricular pace/sense electrodes if an R-wave is not sensed by a ventricular sense amplifier coupled to the ventricular pace/sense electrodes within a ventricular escape interval (V-V interval) timed by a ventricular escape interval timer.
Additionally, a dual chamber, demand pacemaker may be implanted into the patient to supply pacing pulses, when required, to one upper heart chamber and to one lower heart chamber, typically the right atrium and the right ventricle. In a dual chamber, demand pacemaker operating in a DDD pacing mode, both the AAI and VVI modes are followed, under the above defined conditions. A ventricular pacing pulse is delivered to the ventricular pace/sense electrodes if an R-wave is not sensed by the ventricular sense amplifier coupled thereto within an AV time interval timed from the sensing of a P-wave by the atrial sense amplifier.
Over the years, it has been proposed that various conduction disturbances involving both the bradycardia and the tachycardia of the heart chamber could benefit from stimulation applied at multiple electrode sites positioned in or about it in synchrony with a depolarization which has been sensed at least one of the electrodes sites. In addition, it has been proposed to employ pacing to compensate for conduction defects and in congestive heart failure where depolarizations that naturally occur in one upper or lower chamber are not conducted quickly enough to the other upper or lower heart chamber. In such cases, the right and left heart chambers do not contract in optimum synchrony with each other, and the cardiac output suffers due to the timing imbalance. In other cases, spontaneous depolarizations of the left atrium or left ventricle occur at ectopic foci in these left heart chambers, and the natural activation sequence is grossly disturbed. In such cases, cardiac output deteriorates because the contraction of the right and left heart cambers are not synchronized sufficiently to eject blood therefrom.
In patients suffering from congestive heart failure, the hearts become dilated and the conduction and depolarization sequences of the heart chambers may exhibit Intra-Atrial Conduction Defects (IACD), Left Bundle Branch Block (LBBB), Right Bundle Branch Block (RBBB) and Intra Ventricular Conduction Defects (IVCD). Single and dual chamber pacing of the right atrium and/or the right ventricle can be counterproductive in such cases, depending on the defective conduction pathway and the location of the pace/sense electrodes.
A number of proposals have been advanced for providing pacing therapies to alleviate theses conditions and restore synchronous depolarization of right and left, upper and lower, heart chambers. The proposals appearing in U.S. Pat. Nos. 3,937,266, 4,088,140, 4,548,203, 4,458,677 and 4,332,259 are summarized in U.S. Pat. Nos. 4,928,688 and 5,674,259, all incorporated herein by reference. The advantages of providing sensing at pace/sense electrodes located in both the right and left heart chambers are addressed in the ""688 and ""259 patents, as well as in U.S. Pat. Nos. 4,354,497, 5,174,289, 5,267,560, 5,514,161, 5,584,867, also all incorporated herein by reference. Typically, the right atrium is paced at expiration of an A-A escape interval, and the left atrium is simultaneously paced or synchronously paced after a short delay time. Similarly, the right ventricle is paced at expiration of a V-V escape interval, and the left ventricle is simultaneously paced or synchronously paced after a short delay. Some of these patents propose limited forms of DDD pacing having xe2x80x9cbi-ventricularxe2x80x9d or xe2x80x9cbi-atrialxe2x80x9d demand or triggered pacing functions. In all cases, a pacing pulse delivered at the end of the escape internal or AV delay (a xe2x80x9cpaced eventxe2x80x9d) triggers the simultaneous or slightly delayed delivery of the pacing pulse to the other heart chamber. They do not propose pacing a right or left heart chamber at the end of the escape interval or AV delay and then inhibiting pacing in the other of the right or left heart chamber if a conducted depolarization is detected in that other heart chamber within a physiologic time related to the location of the pace/sense electrodes.
In the ""259 patent, a combined epicardial IPG and electrode array are proposed for fitting about the apical region of the heart and providing a VVI pacing function providing for substantially simultaneous depolarization of both ventricles through selected ones of the pace/sense electrodes on time out of a V-V escape interval. It is not clear what occurs if an R-wave is sensed at one of the left or right ventricular pace/sense electrodes within the V-V escape interval.
In the ""688 patent, two- or three-chamber pacing systems are disclosed wherein a programmable synchronization time window of about 5-10 msec duration is started on the sensing of an R-wave or a P-wave at pace/sense electrodes in one of the ventricles or atria before the expiration of a V-V or an A-A escape interval, respectively. The delivery of the pacing pulse in the other atrium or ventricle is inhibited if a P-wave or an R-wave is sensed at the pace/sense electrode site in that chamber within the synchronization time window in atrial or ventricular pace/sense electrodes if the V-V escape interval times out without sensing a P-wave or an R-wave at either pace/sense electrode site. In a DDD pacemaker context, an atrial pace/sense electrode, sense amplifier and pace output circuit and a pair of ventricular pace/sense electrodes, sense amplifiers and pace output circuits are provided. The AV delay timer is started when a P-wave is sensed, and ventricular pacing pulses are preferably supplied simultaneously to the two ventricular pace/sense electrodes if an R-wave is not sensed by either ventricular sense amplifier before the AV delay times out.
A double atrial, triple chamber pacing system is described in the ""161 and ""867 patents. Such a pacing system is used for treating dysfunctional atrial conduction using a programmable DDD pacemaker for pacing both atria simultaneously when an atrial sensed event is detected from either chamber or at the expiration of a V-A escape interval. The IPG includes atrial sense amplifiers coupled to atrial pace/sense electrodes positioned with respect to electrode sites in or adjacent the right and left atria and a ventricular sense amplifier coupled to ventricular pace/sense electrodes located in or on the right ventricle. In the ""161 patent, ventricular pacing pulses are applied to the ventricular pace/sense electrodes at the end of an AV delay timed from the atrial paced events unless the sensed atrial rate exceeds a rate limit. In the ""867 patent, a fall back mode is commenced to limit the ventricular pacing rate if the sensed P-wave are deemed xe2x80x9cprematurexe2x80x9d. Clinical experience in use of double atrial, three chamber, pacing systems appears in abstracts by Daubert et al., including xe2x80x9cPermanent Dual Atrium Pacing in Major Intratrial Conduction Blocks: A Four Years Experiencexe2x80x9d appearing in PACE (Vol.16, Part II, NASPE Abstract 141, p. 885, April 1993). In these systems, atrial pacing pulses are delivered simultaneously in a triggered mode to both atria that is wasteful of electrical energy and fails to maintain a physiologic delay between the evoked depolarizations of the atria.
Further clinical experience with two, three and four heart chamber pacing is also reported by Daubert et al. in xe2x80x9cPermanent Left Ventricular Pacing With Transvenous Leads Inserted Into The Coronary Veinsxe2x80x9d appearing in PACE (Vol. 21, Part II, pp. 239-245, January 1998). In the two heart chamber context, there is disclosed a method of implanting conventional DDDR IPGs with the atrial pace/sense terminals coupled to a left ventricular lead having pace/sense electrodes located in relation to the left ventricle. The ventricular pace/sense terminals were coupled to right ventricular leads having pace/sense electrodes located in relation to the right ventricle. The IPG was programmed to operate in the WIR mode with short AV delays, e.g. 30 ms, for timing delivery of a pacing pulse to the right ventricle when an R-wave was first sensed in or a pacing pulse was delivered to the left ventricle at the end of the programmed V-A escape interval. In this bi-ventricular pacing system, ventricular pacing pulses were not delivered in a triggered mode to both ventricles, but only the conduction delay from the left ventricle to the right ventricle could be programmed.
Also disclosed is the use of a double ventricular, triple chamber pacing system in the above article using DDDR IPGs having the atrial terminals coupled with the atrial pacing lead and the ventricular terminals coupled through an adaptor to two ventricular pacing leads. The pace/sense electrodes of the atrial pacing lead were implanted apparently in relation to the right atrium and the pace/sense electrodes of the ventricular pacing leads were implanted in relation to the right and left ventricles. The DDDR IPG was programmed in the DDDR mode to provide simultaneous pacing of the right and left ventricles at the end of an A-V delay timed from an atrial paced event at the expiration of the V-A pacing escape interval or an atrial sensed event occurring during the V-A escape interval. In this system, the simultaneous delivery of ventricular pacing pulses to both ventricles is wasteful of electrical energy and fails to maintain a physiologic delay between the evoked depolarizations of the ventricles.
A four chamber DDD pacing system providing right and left chamber pacing and sensing is described in the above article, and in an article by Cazeau et al., entitled xe2x80x9cFour Chamber Pacing in Dilated Cardiomyopathyxe2x80x9d appearing in PACE (Vol. 17, Part II, pp. 1974-1979, November 1994). In these and other four chamber systems, right and left atrial leads are coupled xe2x80x9cin seriesxe2x80x9d through a bifurcated bipolar adaptor with atrial pace/sense connector block terminals, and right and left ventricular leads are coupled xe2x80x9cin seriesxe2x80x9d through a bifurcated bipolar adaptor with ventricular pace/sense connector block terminals. Right atrial and right ventricular leads are connected to the cathode ports, while left atrial and left ventricular leads are connected to the anode ports of each bipolar bifurcated adaptor. The IPG is programmed in the DDD mode and in a bipolar pacing mode with a common AV delay that is connected by the delivery of atrial pacing pulses. The earliest right or left atrial sensed event (i.e., the P-wave) within a V-A escape interval or the expiration of the V-A escape interval triggers delivery of atrial pacing pulses to both of the pace/sense electrodes in both atrial chambers through the series connected, right and left atrial leads. It appears that the sensing xe2x80x9cin seriesxe2x80x9d of either a right or left ventricular R-wave across the right and left pace/sense electrode during the AV delay terminates the AV delay and triggers delivery of ventricular pace pulses across the right and left pace/sense electrode pair. In this pacing system, both atrial and ventricular pacing pulses are delivered to both atria and both ventricles on the sensing the P-wave and on the sensing R-wave, respectively, which is wasteful of electrical energy. Furthermore, the resulting simultaneous depolarization of the right and left atria or the right and left ventricles in not physiologically beneficial in many instances.
In these approaches, the atrial and/or ventricular pace/sense electrodes are located in a variety of locations and manner with respect to the right and left atria and/or the right and left ventricles. In the ""688 patent, one ventriclar pace/sense electrode is located at the distal end of an endocardial lead introduced deeply into the great vein extending from the coronary sinus to place it adjacent to the left ventricle. It is also known that pace/sense electrode of an endocardial lead can be placed closer to the entrance to the coronary sinus and adjacent the left atrium. Such an approach is shown in the above referenced Cazeau et al. article and in an abstract by Daubert et al., xe2x80x9cRenewal of Permanent Left Atrial Pacing via the Coronary Sinusxe2x80x9d, appearing in PACE (Vol. 15, Part II, NASPE Abstract 255, p. 572, April 1992), also incorporated herein by reference. Epicardial screw-in, pace/sense electrodes can also be placed epicardially on the right and left ventricles because the myocardial walls are thick enough to not be perforated in the process as also shown in the above referenced Cazeau article. In addition, a bi-ventricular pacemaker is proposed in the above-incorporated ""259 patent having an array of ventricular pace/sense electrodes fitting about the apex of the heart to provide a plurality of usable epicardial pacing and/or sensing electrode sites about the apical region of the heart.
Additionally, xe2x80x9cCoronary Sinus Pacing Prevents Induction of Atrial Fibrillation,xe2x80x9d by Papageorgiou et al., proposes a simultaneous high right atrial and coronary sinus pacing to prevent the induction of atrial fibrillation. That is, Papageorgiou proposes that distal coronary sinus pacing suppresses the propensity of high right atrial extra stimulus to induce atrial fibrillation by limiting their prematurity at the posterior triangle of Koch, while not allowing local conduction delay and local reentry to occur.
Furthermore, in xe2x80x9cMultiple Channel, Sequential, Cardiac Pacing Systems,xe2x80x9d Struble et al. discloses an invention directed to providing symmetrically operating left and right heart chamber pacing systems. The pacing systems described in Struble overcome the problems and limitations, disclosed and described above, and provide a great deal of flexibility in tailoring the delivered pacing therapy to needs of the individual patient""s heart.
Finally, in the Diva Functional Product Description, Regarding PVC synchronous atrial stimulation, a Vitatron device allows for PVC synchronous pacing. That is, when the mode of the pacing system is programmed to xe2x80x98On,xe2x80x99 the PVC synchronous atrial pacing feature paces the atrium of the patient""s heart within 20 ms after recording a single PVC event. Furthermore, no atrial pacing function is released from the pacing system within a predetermined period of time from the last event, and the PVC synchronous atrial pacing feature is limited to the first PVC in a row of PVCs.
As discussed above, the most pertinent prior art patents are shown in the following table:
All the patents listed in Table 1 are hereby incorporated by reference herein in their respective entireties. As those of ordinary skill in the art will appreciate readily upon reading the Summary of the Invention, the Detailed Description of the Preferred Embodiments and the Claims set forth below, many of the devices and methods disclosed in the patents of Table 1 may be modified advantageously by using the teachings of the present invention.
The present invention is therefore directed to providing a method and system for instantaneously stimulating the contraction of an atrium of a mammalian heart. Such a system of the present invention overcomes the problems, disadvantages and limitations of the prior art described above, and provides a more efficient and accurate means of immediately contractually stimulating the left atrium of a mammalian heart.
The present invention has certain objects. That is, various embodiments of the present invention provide solutions to one or more problems existing in the prior art respecting the instantaneous stimulation of the contraction of an atrium of a mammalian heart. Those problems include, without limitation: a time delay between the recording of a premature atrial contraction in a first atrium and the stimulation in a second atrium, the recording of a premature atrial contraction in the right atrium and the stimulation of the left atrium upon the above-noted recording.
In comparison to known techniques for stimulating the contraction of an atrium of a mammalian heart, various embodiments of the present invention may provide one or more of the following advantages: the instantaneous stimulation of a second atrium of a mammalian heart, the recording of a premature atrial contraction in the right atrium and the stimulation of the left atrium upon the above-noted recording.
Some of the embodiments of the present invention include one or more of the following features: an implantable medical device including at least one sensing lead, at least one pacing lead, a microprocessor and an input/output circuit including a digital controller/timer circuit, an output amplifier, a sense amplifier, a peak sense and threshold measurement device, a comparator and an electrogram amplifier.
Furthermore, in accordance with the present invention, an embodiment providing for a method and system of stimulating a mammalian heart is provided. This embodiment provides a processor contained within an implantable medical device monitors the intervals between successive beats of the mammalian heart. The processor then measures the interval times and furthermore calculates an average interval time. When one of the interval times is substantially less than the average interval time, the processor will classify that particular interval as containing a premature atrial contraction. When a premature atrial contraction has been detected, the processor will transmit a signal to the left atrium, instructing the left atrium to contract. As a result, the left atrium contracts immediately after the detection of the premature atrial contraction, thereby negating and preventing the start of an atrial tachyarrhythmia.
Therefore, the algorithm of the present invention enables the implantable medical device to trigger the stimulation of the right atrium in response to spontaneous activity sensed by the electrode in the coronary sinus. In this way, it is possible to synchronize the left and right atria in reaction to any spontaneous activity that is sensed. As a result, this mode of pacing may therefore prevent the start of atrial tachyarrhythmia.